igmentar f P y D l o is a o n r r d e u r o s J Bagherani et al., Pigmentary Disorders 2015, 2:10 Journal of Pigmentary Disorders DOI: 10.4172/2376-0427.1000216 World Health Academy ISSN: 2376-0427 Review Open Access An Overview on Melasma Nooshin Bagherani1*, Serena Gianfaldoni2 and Bruce Smoller3 1Dermatologist, Dr. Nooshin Bagherani’s office, Taha Physicians’Building, Khoramshahr, Khuzestan Province, Iran 2Dermatologist, Department of Dermatology, University of PisaVia Roma, 67, 56100 Pisa, Italy 3Professor and chair, Department of Pathology, Department of Dermatology, University of Rochester, School of Medicine and Dentistry, USA Corresponding author: Nooshin Bagherani, Nooshin Bagherani’s office, Taha Physicians’ Building, Khoramshahr, Khuzestan Province, Iran, 00989165828461; E-mail: [email protected] Rec date: July 31, 2015; Acc date: September 26, 2015; Pub date: September 30, 2015 Copyright: © 2015 Bagherani et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited. Abstract Melasma is a common pigmentary skin disorder, characterized by symmetrically-distributed hyperpigmented patches with serrated, irregular and geographic borders. It usually affects the chronically photo-exposed cutaneous areas, especially the face and neck. Its exact worldwide prevalence is unknown. The disease most commonly occurs in women of reproductive ages. The etio-pathogenesis of melasma is not completely understood. This disorder seems to be an interplay of various internal and environmental factors. Among these factors, genetic predisposition, sunexposure and hormonal factors are the most important ones. In this article, in addition to the introduction of melasma, we have tried to review the most effective medications and modalities for the treatment of this common, refractory, pigmentary disorder. Keywords: Melasma; Pigmentation; Pathogenesis; Treatment Asian and Afro-descendant. The age of onset is usually between 30-55 years; rarely the disease has been described during puberty or in post- Introduction menopausal period [4,5]. Melasma is an acquired,chronic,recurrent hyperpigmentary Etiology and Pathogenesis disorder. The word “melasma” is derived from the Greek “melas”, which means black color. The condition is also known as “chloasma”, The etio-pathogenesis of melasma is complex and not completely another Greek term which means green in color, or mask of pregnancy, understood. It appears that this disorder is an interplay of various referring to the high prevalence of the disease in pregnant women. internal and environmental factors, which may be responsible in Melasma is clinically characterized by symmetric light-brown to triggering, maintaining or relapsing lesions. Among these factors, bluish-gray macules and patches, with irregular,sharp borders. The genetic predisposition, sun-exposure and hormonal factors are the pigmentation may be guttate, linear or confluent [1,2]. most important ones, all of which significantly increase the tyrosinase activity [6]. Melasma usually affects the chronically photo-exposed cutaneous areas, especially the face and neck. On the face, the forehead, cheeks, Genetic predisposition has been suggested by the evidence of a temples, upper lip, chin or nose are commonly involved. More rarely, familial history and the association with particular races [7]. Studies lesions may afflict extensor arms and sternal region. Although this have shown that the genes related to lipid metabolism such as PPARα, disorder has been considered a benign condition, which usually has ALOX15B, DGAT2L3 and PPARGC1A are less expressed in melasma only aesthetic implication, it may affect self- image and self-esteem, [8]. with a negative impact on patient’s quality of life [1,2]. The role of the UVR has been well established in the development of melasma. This role is supported by the following points: Epidemiology Localization of the lesions on the sun-exposed areas Melasma is a common pigmentary disorder, affecting about 5-6 million individuals in the United States. However, its exact worldwide The higher prevalence of melasma in the world areas of intense prevalence is unknown. It can affect patients of both sexes and of all UVR races and ages. The disease is most commonly described in women of Accentuation of the lesions in the summers and their attenuation in reproductive ages. In men, melasma is rare and represents less than the winters [7,8] 10% of all cases [3]. Effectiveness of the broad-spectrum sunscreens in preventing and Melasma is more common in darker-skinned patients with treating melasma, Fitzpatrick skin types IV to VI, who live in world areas of high- intensity ultraviolet radiation (UVR). It is more prevalent in Hispanic, The immunoistochemical features of cutaneous sun damage (e.g. solar elastosis) [7] Pigmentary Disorders Volume 2 • Issue 10 • 1000216 ISSN:2376-0427 JPD, hybrid open access journal Citation: Bagherani N, Gianfaldoni S, Smoller B (2015) An Overview on Melasma. Pigmentary Disorders 2: 218. doi:10.4172/2376-0427.1000216 Page 2 of 18 Studies have shown that whole sun-light spectrum including UVA even normal black skin [20]. These pendulous cells can easily drop into (320-400 nm), UVB (290-320 nm) and visible light are important in dermis [11]. the pathogenesis of melasma [9]. They act through the following mechanisms: Increasing the melanocyte proliferation and activity Promoting transfer of the melanin pigments to the keratinocytes [10] Promoting inflammatory mediators [10,11]: The UVR causes peroxidation of lipids in the cellular membranes, leading to generation of free radicals, which promotes the melanocytes to produce excess melanin [9-11]. Up-regulating expression of the melanogenic mediators from the keratinocytes and dermal stem cells [11,12]: The UVR induces production of alpha-melanocyte stimulating hormone [α-MSH],which lead to an increased melanocytosis and melanogenesis [10- 12]. Up-regulating protease-activated-receptors [11] Inducing angiogenesis [12] The female sex hormonal activity has an important role in the Figure 1: Pathology of melasma. pathogenesis of melasma, especially in women. The association of this disorder with pregnancy,oral contraceptive pills and hormone replacement therapies in post-menopausal, is well-known [13]. Studies have shown that melanogenesis is stimulated by the luteinizing In the dermis, melanin pigments are seen in two forms: hormone (LH), follicle-stimulating hormone (FSH) [13] and placental Mainly in macrophages (melanophages) and sphingolipids [14]. As free melanin deposits around the superficial and deep dermal Histopathology vascular plexuses [15]. However, it appears that the significance of dermal melanin in melasma is controversial, because some studies Generally, the histopathological features of melasma per se are have shown that the amount of dermal melanin, in comparison with subtle, so that control skin biopsies are necessary for comparison and the perilesional normal skin is not significant. Moreover, while dermal subsequent diagnosis [15]. melanin is less detectable in Caucasian melisma and frequently found In this disorder, rete ridge flattening and epidermal thinning have in melasma patients with Fitzpatrick skin types III to V, it is detectable been observed [16]. Studies have shown that the epidermal as the normal findings in the normal facial skin of some races such as melanocytes in the lesional skin are more active than that in the Korean and Japanese. On the other hand, it has been suggested that normal skin [9,17-26]; hence, the increased epidermal melanin is its alterations in dermal structures has a role in the melasma pathological hallmark [18,22,23], seen significantly in the basal and development, so that a network of cellular interactions between the suprabasal cells as pigmentary caps [9,15] (Figure 1). In some studies, fibroblasts, vasculatures and melanocytes during the chronic sun this finding has been observed in all layers of the epidermis [15]. exposure can lead to stimulating the melanocytes [18]. Moreover, the stratum corneum is thinned [16] and in some cases, In melasma, some non-specific changes can be observed such as degraded molecules of the melanin have been observed in this layer solar elastosis [15,16,18-23], increased vasculature and telangiectasia [27] using Masson Fontana for staining the melanin pigments [15,22]. [15,16,18,20-22,29]. Solar elastosis, a predominant findings in the For showing increased melanocytic activity, the Mel-5 immuno- melasma lesions [18], is seen as clumps of thick and fragmented elastic staining is administered [15]. More precise assessment shows enlarged, fibers in the papillary dermis,stained with Verhoeff-van Gieson [15]. intensely stained melanocytes with prominent dendrites In this pigmentary disorder, there is a mild perivascular [15,17,20-23,28]. lymphohistiocytic infiltrate [28]. In contrast to post inflammatory Assessment of the basement membrane shows that it is disrupted in hyperpigmentation [PIH], there is no apparent inflammatory phase in melasma and in comparison with the normal perilesional skin, all stages of its development [30]. expresses significantly less of the type IV collagen and markedly more Immunohistochemistry studies have shown that the number of of the MMP2 protein and mRNA [18,20]. Moreover, the staining is epidermal melanocytes can be both increased